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Genetics and Epigenetics of Aging
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Genetics and Epigenetics of Aging

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 February 2023) | Viewed by 19919

Special Issue Editors

Prof. Dr. Xiao-Li Tian

E-Mail Website
Guest Editor
Department of Human Population Genetics, Human Aging Research Institute (HARI) and School of Life Sciences, Nanchang University, Nanchang 330031, China
Interests: poluation genetics; cardiovascular diseases; longevity; epigenetic; vascular aging; hypertension; atherosclerosis
Prof. Dr. Ting Ni

E-Mail Website
Guest Editor
School of Life Sciences, Fudan University, Shanghai 200438, China
Interests: cell senescence; aging; RNA; gene regulation; alternative splicing; intron retention; alternative polyadenylation; 3′ UTR

Special Issue Information

Dear Colleagues,

Aging is an independent risk for many common diseases, such as cardiovascular diseases, cancers, and dementia. It is known that genetic, epigenetic, and environmental factors affect the aging process profoundly. Over the past decades, candidate approach, particularly in multiple omics tools, such as genome-wide association, methylation, chromatin conformation, RNA sequencing, and all types of proteomics, have been used in the search of genes and epigenetic changes, including their interactions with environmental factors associated with aging and age-related diseases at the genome level. This provides a comprehensive view on the aging process, both temporally and spatially. Integration of these omics data with functional assessments has provided a unique tool to define and interpret the effects of genetic variance and epigenetic alteration on the aging process.  For instance, a number of genetic and epigenetic markers and signaling pathways, including those in mitochondrion, were found to estimate or explain the mechanisms on aging and longevity. These provocative findings  help to gain new insights into the aging process, i.e., the old myth.

In this Special Issue, we would like to invite submissions of original research or review articles on the topics relevant to “Genetics and Epigenetics of Aging”. We believe that this knowledge will help researchers and general readers understand how genetic and epigenetic changes affect aging and how we can possibly take advantage of these efforts to eradicate age-related diseases, extending our healthspan. We look forward to receiving your contributions.

Prof. Dr. Xiao-Li Tian
Prof. Dr. Ting Ni
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • aging
  • senescence
  • genetic
  • epigenetic
  • mutation
  • gene expression
  • signaling pathway
  • age-related diseases
  • longevity

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Published Papers (6 papers)

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Research

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16 pages, 2886 KiB  
Article
The Role of Alternative Splicing Factors, DDB2-Related Ageing and DNA Damage Repair in the Progression and Prognosis of Stomach Adenocarcinoma Patients
by Xinshu Wang, Zhiyuan Huang, Lei Li, Yuntong Yang, Jiyuan Zhang, Li Wang, Jian Yuan and Yunhui Li
Genes 2023, 14(1), 39; https://doi.org/10.3390/genes14010039 - 23 Dec 2022
Cited by 5 | Viewed by 1698
Abstract
DNA damage response is a key signal transduction pathway in triggering ageing and tumor progression. Abnormal alternative splicing (AS) is associated with tumors and ageing. However, the role of AS factors associated with DNA damage repair and ageing in stomach adenocarcinoma (STAD) remains [...] Read more.
DNA damage response is a key signal transduction pathway in triggering ageing and tumor progression. Abnormal alternative splicing (AS) is associated with tumors and ageing. However, the role of AS factors associated with DNA damage repair and ageing in stomach adenocarcinoma (STAD) remains unclear. We downloaded the percentage of splicing (PSI) values for AS in STAD from the TCGA SpliceSeq database. The PSI values of DNA repair gene AS events were integrated with STAD patient survival data for Cox regression analysis. The prediction model for the overall survival (OS) was constructed by the clinical traits. The tumor immune microenvironment was analyzed by CIBERSORT and ESTIMATE. We detected 824 AS events originating from 166 DNA repair genes. Cox regression analysis provided 21 prognostic AS events connected with OS statistically, and a prognostic prediction model was constructed. The expression of these AS factors was higher in STAD tumors. DDB2 high senescence levels were associated with active immune responses and better survival in STAD patients. We built a novel prognostic model founded on DNA repair genes with AS events and identified that DDB2 may be a potential biomarker to apply in clinics. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Aging)
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15 pages, 7777 KiB  
Article
ASH2L Aggravates Fibrosis and Inflammation through HIPK2 in High Glucose-Induced Glomerular Mesangial Cells
by Wen Zhong, Chen Hong, Yejun Dong, Yuhui Li, Chenxi Xiao and Xinhua Liu
Genes 2022, 13(12), 2244; https://doi.org/10.3390/genes13122244 - 29 Nov 2022
Cited by 5 | Viewed by 1752
Abstract
Diabetic nephropathy (DN) is a leading cause of end-stage renal disease and continues to be a threat to patients with diabetes. Dysfunction of glomerular mesangial cells (GMCs) is the main contributing factor to glomerulosclerosis, which is a pathological feature of DN. The epigenetic [...] Read more.
Diabetic nephropathy (DN) is a leading cause of end-stage renal disease and continues to be a threat to patients with diabetes. Dysfunction of glomerular mesangial cells (GMCs) is the main contributing factor to glomerulosclerosis, which is a pathological feature of DN. The epigenetic factor ASH2L has long been thought to be a transcriptional activator, but its function and involvement in diabetic nephropathy is still unclear. Here, we investigated the effect of ASH2L on the regulation of fibrosis and inflammation induced by high glucose in mouse mesangial cells (mMCs). We observed that ASH2L expression is increased in high glucose-induced mMCs, while loss of ASH2L alleviated fibrosis and inflammation. Furthermore, ASH2L-mediates H3K4me3 of the homeodomain-interacting protein kinase 2 (HIPK2) promoter region, which is a contributor to fibrosis in the kidneys and promotes its transcriptional expression. Similar to loss of ASH2L, silencing HIPK2 also inhibited fibrosis and inflammation. In addition, ASH2L and HIPK2 are upregulated in the kidneys of both streptozocin-induced and db/db mouse. In conclusion, we uncovered the crucial role of ASH2L in high glucose-induced fibrosis and inflammation, suggesting that ASH2L regulation may be an attractive approach to attenuate the progression of DN. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Aging)
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14 pages, 3671 KiB  
Article
Alteration of E2F2 Expression in Governing Endothelial Cell Senescence
by Hongfei Liu, Liping Chen, Wanli Xiao, Jiankun Liu, Changkun Long, Wenxing Zhan, Cui Cui, Lin Yang and Shenghan Chen
Genes 2022, 13(9), 1522; https://doi.org/10.3390/genes13091522 - 24 Aug 2022
Cited by 7 | Viewed by 2791
Abstract
Endothelial cell senescence has a vital implication for vascular dysfunction, leading to age-related cardiovascular disease, especially hypertension and atherosclerosis. E2F transcription factor 2 (E2F2) plays a critical role in cell proliferation, differentiation, and DNA damage response. Up to date, no study has ever [...] Read more.
Endothelial cell senescence has a vital implication for vascular dysfunction, leading to age-related cardiovascular disease, especially hypertension and atherosclerosis. E2F transcription factor 2 (E2F2) plays a critical role in cell proliferation, differentiation, and DNA damage response. Up to date, no study has ever connected E2F2 to vascular endothelial cell senescence. Here, we demonstrate that E2F2 is involved in endothelial cellular senescence. We found that E2F2 expression is decreased during the replicative senescence of human umbilical vein endothelial cells (HUVECs) and the aortas of aged mice. The knockdown of E2F2 in young HUVECs induces premature senescence characterized by an increase in senescence-associated β-galactosidase (SA-β-gal) activity, a reduction in phosphorylated endothelial nitric oxide synthase (p-eNOS) and sirtuin 1 (SIRT1), and the upregulation of senescence-associated secretory phenotype (SASP) IL-6 and IL-8. The lack of E2F2 promoted cell cycle arrest, DNA damage, and cell proliferation inhibition. Conversely, E2F2 overexpression reversed the senescence phenotype and enhanced the cellular function in the senescent cells. Furthermore, E2F2 deficiency downregulated downstream target genes including CNNA2, CDK1, and FOXM1, and overexpression restored the expression of these genes. Our findings demonstrate that E2F2 plays an indispensable role in endothelial cell senescence. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Aging)
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10 pages, 2475 KiB  
Article
Specific Gain and Loss of Co-Expression Modules in Long-Lived Individuals Indicate a Role of circRNAs in Human Longevity
by Ming-Xia Ge, Jian-Jun Jiang, Li-Qin Yang, Xing-Li Yang, Yong-Han He, Gong-Hua Li and Qing-Peng Kong
Genes 2022, 13(5), 749; https://doi.org/10.3390/genes13050749 - 24 Apr 2022
Cited by 2 | Viewed by 2547
Abstract
Deep RNA sequencing of 164 blood samples collected from long-lived families was performed to investigate the expression patterns of circular RNAs (circRNAs). Unlike that observed in previous studies, circRNA expression in long-lived elderly individuals (98.3 ± 3.4 year) did not exhibit an age-accumulating [...] Read more.
Deep RNA sequencing of 164 blood samples collected from long-lived families was performed to investigate the expression patterns of circular RNAs (circRNAs). Unlike that observed in previous studies, circRNA expression in long-lived elderly individuals (98.3 ± 3.4 year) did not exhibit an age-accumulating pattern. Based on weighted circRNA co-expression network analysis, we found that longevous elders specifically gained eight but lost seven conserved circRNA-circRNA co-expression modules (c-CCMs) compared with normal elder controls (spouses of offspring of long-lived individuals, age = 59.3 ± 5.8 year). Further analysis showed that these modules were associated with healthy aging-related pathways. These results together suggest an important role of circRNAs in regulating human lifespan extension. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Aging)
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Review

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19 pages, 2115 KiB  
Review
New Insights into the Genetics and Epigenetics of Aging Plasticity
by Jie Zhang, Shixiao Wang and Baohua Liu
Genes 2023, 14(2), 329; https://doi.org/10.3390/genes14020329 - 27 Jan 2023
Cited by 4 | Viewed by 4666
Abstract
Biological aging is characterized by irreversible cell cycle blockade, a decreased capacity for tissue regeneration, and an increased risk of age-related diseases and mortality. A variety of genetic and epigenetic factors regulate aging, including the abnormal expression of aging-related genes, increased DNA methylation [...] Read more.
Biological aging is characterized by irreversible cell cycle blockade, a decreased capacity for tissue regeneration, and an increased risk of age-related diseases and mortality. A variety of genetic and epigenetic factors regulate aging, including the abnormal expression of aging-related genes, increased DNA methylation levels, altered histone modifications, and unbalanced protein translation homeostasis. The epitranscriptome is also closely associated with aging. Aging is regulated by both genetic and epigenetic factors, with significant variability, heterogeneity, and plasticity. Understanding the complex genetic and epigenetic mechanisms of aging will aid the identification of aging-related markers, which may in turn aid the development of effective interventions against this process. This review summarizes the latest research in the field of aging from a genetic and epigenetic perspective. We analyze the relationships between aging-related genes, examine the possibility of reversing the aging process by altering epigenetic age. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Aging)
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21 pages, 1292 KiB  
Review
Recent Advances in Epigenetics of Age-Related Kidney Diseases
by Feng Liu, Jiefang Chen, Zhenqiong Li and Xianfang Meng
Genes 2022, 13(5), 796; https://doi.org/10.3390/genes13050796 - 29 Apr 2022
Cited by 8 | Viewed by 5440
Abstract
Renal aging has attracted increasing attention in today’s aging society, as elderly people with advanced age are more susceptible to various kidney disorders such as acute kidney injury (AKI) and chronic kidney disease (CKD). There is no clear-cut universal mechanism for identifying age-related [...] Read more.
Renal aging has attracted increasing attention in today’s aging society, as elderly people with advanced age are more susceptible to various kidney disorders such as acute kidney injury (AKI) and chronic kidney disease (CKD). There is no clear-cut universal mechanism for identifying age-related kidney diseases, and therefore, they pose a considerable medical and public health challenge. Epigenetics refers to the study of heritable modifications in the regulation of gene expression that do not require changes in the underlying genomic DNA sequence. A variety of epigenetic modifiers such as histone deacetylases (HDAC) inhibitors and DNA methyltransferase (DNMT) inhibitors have been proposed as potential biomarkers and therapeutic targets in numerous fields including cardiovascular diseases, immune system disease, nervous system diseases, and neoplasms. Accumulating evidence in recent years indicates that epigenetic modifications have been implicated in renal aging. However, no previous systematic review has been performed to systematically generalize the relationship between epigenetics and age-related kidney diseases. In this review, we aim to summarize the recent advances in epigenetic mechanisms of age-related kidney diseases as well as discuss the application of epigenetic modifiers as potential biomarkers and therapeutic targets in the field of age-related kidney diseases. In summary, the main types of epigenetic processes including DNA methylation, histone modifications, non-coding RNA (ncRNA) modulation have all been implicated in the progression of age-related kidney diseases, and therapeutic targeting of these processes will yield novel therapeutic strategies for the prevention and/or treatment of age-related kidney diseases. Full article
(This article belongs to the Special Issue Genetics and Epigenetics of Aging)
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